It is becoming clear that multiple forms of cognitive ability or susceptibility to neurodegenerative disorders are affected by general systemic metabolic function. Thus, cognitive health is tightly linked to metabolic health. Previously, we have already pioneered this work by linking the progression of Huntingtons disease to a diabetic-like state. It is clear from several lines of evidence, including our own, that hormones responsible for metabolic regulation also play vital roles in cognitive function. For example, we have previously shown that Exendin-4, which is a long-acting analogue of the gut hormone Glucagon-like peptide 1 (GLP-1) can improve euglycemia, protect pancreatic islet function, improve motor coordination and reduce mutant huntingin aggregates in a mouse model of Huntingtons disease. It is likely that through the creation of multiple types of metabolically-targeted therapeutics, there will also be the creation of distinct mechanisms by which these strategies affect cognitive function. Currently we are investigating underlying metabolic dysunction in various neurological disorders, such as Alzheimer's disease, Huntington's disease, Autism Spectrum disorder, Post-partum depression, and WAGR syndrom. Our goal is to first understand how multiple types of glycemic and metabolic control can affect neuronal function and then to tailor distinct novel therapeutics which can maintain or enhance both metabolic and cognitive function.